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. 2021 Jul 7;12:4193. doi: 10.1038/s41467-021-24348-6

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© The Author(s) 2021, corrected publication 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — A Somatic alterations of TGFBR2 and other genes in TGF-β/SMAD pathway. B RISH analysis of TGFBR2 expression in 41 NPCs and 14 adjacent normal epithelium. Significant downregulation of TGFBR2 was observed (Unpaired two-tailed t test, ****p < 0.0001, mean values of the data are presented) in NPC. Representative NPC cases (NPC33T, NPC-52T) showing no TGFBR2 expression in the tumor cells (red arrows) and positive signals in the infiltrating lymphocytes (blue arrows) and normal epithelium (black arrows). Scale bar: 10 μm. C Dramatic growth inhibition was found in wild-type TGFBR2 transfected TGFBR2-deleted NPC43 cells (unpaired two-tailed t test, *p < 0.05; ***p < 0.0005; data are presented as mean values ± SEM). Western blotting showed pSMAD2 and pSMAD3 overexpression in TGFBR2-expressing NPC43 cells. NP460 with TGFBR2 expression was included as control. Replication: n = 3 biologically independent experiments. D Re-introduction of wild-type TGFBR2 induced cell differentiation and morphological changes in NPC43 cells. In TGFBR2-expressing NPC43 cells, the levels of involucrin were increased upon TGF-β1 treatment, as compared with the vector control. Replication: n = 3 biologically independent experiments. Similar results were found in the repeated experiments. Scale bar: 50 μm. E CRISPR/Cas9-mediated knockout of TGFBR2 in NP460 (NP460KO) cells resulted in the loss of TGFBR2. No pSmad2 and pSmad3 expression were detected in NP460KO cells following TGF-β1 treatment. Re-expression of wild-type TGFBR2 in NP460KO cells restored its response to TGF-β1 as shown by the induction of pSmad2 and pSmad3. NP460KO cells showed significant growth inhibition when compared with parental NP460 cells after TGF-β1 treatment (unpaired two-tailed t test, *p < 0.05; ***p < 0.0005; data are presented as mean values ± SEM). Replication: n = 5 biologically independent experiments. F The parental NP460 and NP460KO cells were infected with a GFP-tagged recombinant EBV. After EBV infection and flow sorting of EBV-positive cells, significantly higher numbers of EBV-positive cells were maintained in TGFBR2 knockout NP460KO cells than those in parental cells on both day7 and day 14 (unpaired two-tailed t test, ****p < 0.0005, data are presented as mean values ± SEM). Replication: n = 3 biologically independent experiments. Source data are provided as a Source Data file.